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Biomedical subjects

M Kanno

Publications and source records attributed to M Kanno.

At least 343 records · Page 19Linked to original sources

Inhibitory action of 6-ethyl-3-(1H-tetrazol-5-YL)chromone (AA-344) on IgE, IgGa- or chemical agent-induced histamine release from isolated rat mast cells.

The antiallergic action of 6-ethyl-3-(1H-tetrazol-5-yl)chromone (AA-344) was studied on isolated rat peritoneal mast cells. AA-344 clearly inhibited the IgE-mediated release of histamine caused by various concentrations of antigen and the 50% inhibitory concentration was 0.1 microM. On the IgGa-mediated release of histamine, a peak inhibition of AA-344 was observed at 10 microM. The histamine release induced by chemical agents such as concanavalin A, dextran and compound 48/80 was depressed by AA-344 at the range of 0.1--1 mM. The results obtained in this study indicate that the antiallergic action of AA-344 is due to selective inhibition on the immunological release of the chemical mediator from mast cells.

Animals↗

Hyperbaric oxygen and stellate ganglion blocks for idiopathic sudden hearing loss.

Ninety-one patients suffering from idiopathic sudden hearing loss are presented. Twenty-two patients were given medical treatment (vasodilators, steroid hormones and vitamins) alone (group 1). Forty-nine patients were treated with stellate ganglion block (SGB) plus oxygen hyperbaric therapy (OHP) (group 2) and 20 patients were treated with SGB plus OHP along with medical treatment (group 3). The SGB plus OHP treated patients were given bupivacaine, which induced Moor's anterior approach of SGB and then exposed to oxygen at a pressure of 2.4 ATA for 90 min. In group 1, 69% of the patients treated within one week after onset exhibited over 10 dB pure tone average improvement, with only 33% patients treated one to two weeks after onset experiencing over 10 dB. However, 74% of the patients in group 2 and 100% of the patients in group 3 who were treated within two weeks after onset exhibited over 10 dB improvement. More significantly, of the patients which experienced complete loss of hearing, 83% in group 2 and 100% in group 3, exhibited over 10 dB improvement, compared to only 33% in group 1. Moreover, 8 (40%) patients in group 3 recovered to within 20 dB of their normal hearing levels. In group 2, 17 patients were treated two to six weeks after onset and 12 (71%) patients had over 10 dB improvement. SGB plus OHP therapy was shown effective in the treatment of sudden idiopathic hearing loss even when patients were treated more than two weeks after onset.

Adult↗

Biliary spasmolytic action of 3-(2,4,5-triethoxybenzoyl)propionic acid (AA-149) in dogs.

The spasmolytic action of 3-(2,4,5-triethoxybenzoyl)propionic acid (AA-149) on the biliary tract was investigated in anesthetized dogs. Intravenous administration of AA-149 at 2 mg/kg and higher doses produced a dose-dependent reduction in passage resistance through the choledochoduodenal junction and in gallbladder pressure, and a dose-dependent increase in bile flow. AA-149, like cholecystokinin, decreased biliary ductal pressure in spite of increasing the bile flow in dogs with ligation of the cystic duct of the gallbladder, whereas taurocholate increased the pressure as well as the bile flow. Moreover, the spasmic response of the choledochoduodenal junction to morphine was depressed strongly by AA-149, BUT NOT CONSISTENTLY BY ATROPINE. The effects of AA-149 were not influenced by pretreatment with atropine, phentolamine or propranolol. These findings strongly suggest that AA-149 relaxed the biliary tract and depressed the morphine-induced spasm by a mechanism different from those of anticholinergic and sympathomimetic agents.

Animals↗

A possible mechanism of choleretic action of 3-(2,4,5-triethoxybenzoyl)-propionic acid (AA-149) in dogs.

The choleretic action of 3-(2,4,5-triethoxybenzoyl)propionic acid (AA-149) was studied in anesthetized dogs. AA-149 produced a dose-dependent increase of the bile flow with both i.v. and intrajejunal administration of doses 1 mg/kg and higher. Biliary clearance of 14C-erythritol showed that AA-149 stimulated canalicular bile formation without enhancement of water secretion and/or inhibition of bile reabsorption in the biliary ductules and ducts. AA-149 did not increase the excretion of bile acids into the bile, but enhanced the excretion of the biliary electrolytes, in particular sodium ion, in proportion to an increase of the bile flow. About 3--4% of AA-149 administered i.v. was excreted into the bile during the first 1 h period, so that biliary AA-149 was insufficient to increase the bile flow via its osmotic effect. These results strongly suggest that the choleretic action of AA-149 is attributable to stimulation of a bile acid-independent bile formation in the canaliculi coupled with an active sodium transport system.

Animals↗